Unformatted text preview: BIO 317 EXAM 2 November 9, 2010 Instructions (failure to follow instructions may result in your OPSCAN sheet being
rejected) 1. DO NOT OPEN YOUR EXAM until told to do so by the proctor. 2. Use only a #2 pencil to fill out the OPSCAN sheet and do not forget to blacken all the spots. 3. Fill out your personal information on your OPSCAN sheet NOW. a. Enter your NAME, last name first, in the space indicated at the top of the OPSCAN sheet. b. Enter your SBU ID NUMBER in the space indicated in the lower left corner of the OPSCAN sheet: c. Sign YOUR NAME in the top right margin of the OPSCAN Sheet 4. Do not mark any other spaces (except answers) on the OPSCAN. Questions / Points There are 6 pages with 25 questions worth a total of 100 points on this exam. Each question is worth 4 points. Choose the best answer and mark your answer on the OPSCAN sheet. Answer every question. There is no penalty for guessing. If you must erase, do so carefully and completely. The system is very sensitive and you WILL NOT get credit if it picks-up two or more answers. Also mark your answers on this paper so you can check the key. Answers will be posted on the course BlackBoard web page this afternoon. Grades Grades will be posted on course BlackBoard web page (in the gradebook) as soon as possible. OPSCANS will not be returned. 1) Choose the incorrect statement: a- The dynamic range curve represents the range of stimulus intensities that a specific receptor responds to. b- Sensory receptors encode specific features of a stimulus. c- The fractionation of the dynamic range depends on conformational changes of the receptor itself. d- TRP channels are involved in signal transduction. 2) A receptor cell is: a- The first recipient of the stimulus from the environment. It converts the stimuli into a message for the central nervous system. b- A generator of signals that do not propagate to other cells. c- A cell that conveys information from multiple different sensory receptors and codes for different sensory modalities. d- None of the above 3) The following is true of the function and mechanism of sensory transduction of sensory bristles: a- Sensory bristles transduce auditory stimuli. b- Sensory bristles are present in all mammals and release neuromodulators on receptor cells to encode auditory stimuli. c- Sensory bristles are connected to thermoreceptors. In response to temperature changes they bend in one specific direction and activate ion channels on the receptor cell. d- Sensory bristles bend in response to mechanosensory stimuli. The movement can activate TRPN1 that activate the receptor cell. 4) Sensory systems can respond to complex stimuli by: a- using different G-protein activations. b- using different receptors encoding different properties of the stimulus. c- using a single receptor, which responds to all sensory modalities. d- modifying the site of generation of the action potential. 5) Choose the correct statement: a- Sensory adaptation is the mechanism of generation of action potentials for sensory receptors. b- The opening of ion channels is not necessary to generate an action potential and encode sensory stimuli. c- The crayfish stretch receptors encode mechanical stimuli that arise from the stretching of muscle fibers. d- Hair cells in the basilar membrane are protective structures for the basilar membrane. 6) The following is true about the regulation of
cAMP levels: a) Different G-proteins can either upregulate or downregulate cAMP through activation or inhibition of adenylyl cyclase. b) Caffeine downregulates cAMP by stimulating cAMP-phosphodiesterase. c) Cholera toxin downregulates cAMP by ADP-ribosylation and inhibition of Gs. d) Adenylyl cyclase causes cAMP inactivation by catalyzing its conversion to AMP. e) A cyc- mutant cell would lack adenylyl cyclase and thus overproduce cAMP. 7) The following is true for the Adrenalin Receptor: a) It is a direct receptor, in which ligand binding correlates well with response. b) It contains seven transmembrane domains, which is indicative of a G-protein- linked receptor. c) Overexpression can prevent the formation of activated dimers even with adrenaline binding. d) It can be ADP-ribosylated and inactivated by pertussis toxin, resulting in a block of adrenaline action. e) It can result in the inhibition of adenylyl cyclase in some cells and the stimulation in other cells, depending on which G-protein is expressed. 8) The following is true of receptor-linked G-proteins: a) The same G-protein can directly regulate adenylyl cyclase or phospholipase C. b) They are activated when GTP is broken down to GDP. c) Their existence was suggested by a mutant cell that was not responsive to adrenaline, but still had adrenaline receptors, and did respond to forskolin. d) They have intrinsic GTPase activity that is directly activated by receptor binding. e) Activation involves the liberation of a G-beta/gamma subunit complex bound to GDP. 9) Light: a) stimulates a signaling cascade that results in the closing of sodium channels and hyperpolarization of photoreceptor neurons. b) inhibits guanylyl cyclase production of cGMP, resulting in decreased cGMP levels. c) blocks the activation of GT, leading to guanylyl cyclase inhibition. d) directly gates a photosensitive Na channel. e) initiates a signaling cascade that leads to phosphodiesterase inhibition. 10) The following is true of Rhodopsin: a) It consists of opsin that is covalently linked to cis-retinal. b) It is inactivated by light. c) It is linked to the G-protein-mediated activation of a protein kinase. d) It is a light-gated ion channel for Na+. e) It is regulated by cGMP. 11) The following is true about cGMP phosphodiesterase (PDase) in photoreceptors: a) It blocks the light-mediated opening of sodium channels. b) Its activation results in the opening of sodium channels. c) It is a directly activated effector of the G-protein, Transducin. d) It is most active in the dark. e) It is hyper-activated by forskolin toxin. 12) The following is NOT true of the Phosphatidylinositol (PI) based signaling pathway: a) C-kinase is activated after stimulation of PIP2 breakdown. b) It is stimulated by Gq protein-linked receptors. c) The signaling-active phospholipid is PIP2, in which the inositol head group is highly phosphorylated. d) The generated second messengers are DAG and IP3 , which act at the plasma membrane and the cytoplasmic Ca++ stores, respectively. e) It can result in the stimulation of adenylyl cyclase, but only in cells that contain Gs and lack Gq. 13) The following is NOT true of Phospholipase C involvement in the PI-based signaling pathway: a) It cleaves off the phosphorylated head group from the diacylated fatty acid tail of its substrate phospholipid. b) It is directly activated by Gq. c) It acts on a phosphorylated form of phosphatidylinositol but not of phosphatidylserine. d) It is a plasma membrane bound enzyme. e) None of the above. 14) During adrenaline control of glycogen metabolism a) glycogen synthase is stimulated by phosphorylation. b) phosphorylase kinase inactivates phosphorylase b. c) as a response to stress, glycogen breakdown is inhibited, limiting the production of glucose. d) amplification of the response is achieved at least by activations of many Gs- proteins and protein kinase A-mediated phosphorylation. e) none of the above. 15) The following is true of the regulation of catecholamine metabolism: a) DOPA decarboxylase-mediated production of the first catecholamine (dopamine) is the rate-limiting step. b) Tyrosine hydroxylase is inactivated through cAMP production. c) Catecholamines are caused to stimulates their own production through a positive feedback loop. d) Phosphorylation of tyrosine hydroxylase relieves end product (catecholamine) inhibition and stimulates more production of catecholamines. e) none of the above. 16) The following is NOT true about Calmodulin: a) it can activate or inhibit a variety of enzymes and channels. b) it has two EF hand domains that can each bind up to 2 Ca++ ions. c) it acts as a cellular calcium sensor. d) it wraps around its targets (binding proteins) in the presence of calcium. e) it is a catalytic enzyme, activated by calcium. 17) Protein kinase A (PKA) and protein kinase C (PKC) a) both require Ca++ for their activation b) are normally activated by second messenger-induced release of auto-inhibition. c) are capable of phosphorylating both serines and tyrosines. d) can each be activated in the absence of second messengers. e) are each activated upon membrane binding. 18) The following is NOT true of CaM kinase a) It can bind Ca++ in the absence of binding to calmodulin. b) Autophosphorylation participates in both maximum activation and prolonged activation, even in the absence of binding Ca++ or calmodulin. c) Autophosphorylation induces a confomational change that allows for tighter binding of calmodulin. d) It phosphorylates a wide variety of substrates resulting in stimulation or inhibition of their functional activities. e) Levels of kinase activity are insensitive to the frequency of Ca++ oscillations in cells. 19) The following is NOT true for protein kinases: a) They can be autoinhibited by pseudosubstrate domains. b) They can be activated by second messengers or by other kinases. c) They can be activated or inhibited within G-protein-stimulated pathways. d) Their ability to phosphorylate a substrate depends on the primary, secondary and tertiary structure of the substrate and the spatial distribution of the substrate protein relative to the kinase. e) None of the above. 20) Proto-oncogenes: a) are normal cellular genes encoding key regulatory proteins of growth control that are targets for mutagenesis, resulting in hyperactivity and uncontrolled growth. b) are expressed as a result of tumor formation. c) are all tyrosine kinases. d) are found in sarcoma viruses that cause cellular transformation and tumor growth. e) None of the above. 21) The following is NOT true about the first identified human oncogene, ras. a) ras transfection into normal mouse fibroblasts can result in their transformation into cancerous cells that can cause a tumor in mice. b) It is able to prevent contact-inhibition of cell growth in culture. c) It encodes a mutant, dominant-inhibitory form of Ras, unable to bind to GTP. d) Its discovery showed that cancer can have a genetic basis. e) It showed that human tumors could be caused by mutation of cellular genes. 22) The Ames test for mutagenicity: a) showed that non-smokers have as many mutagens in their urine as smokers. b) is based on the ability of mutagens to prevent bacterial growth when nucleotides are supplied in the growth medium. c) showed that PAH carcinogens are mutagens only after their enzymatic oxidation by the liver. d) showed that cancer can be caused by environmental toxins that don't result in gene mutation. e) none of the above 23) The following is NOT true about the c-Src kinase: a) It can be activated by a protein that binds to both the SH2 and SH3 domains. b) It can be activated by phosphorylation by the protein tyrosine kinase, Csk. c) It is one member of a family of protein kinases that play important roles in the regulation of cell growth, movement and differentiation in a variety of cell types. d) It can be activated by deletion of tyrosine 527. e) It plays a post-synaptic role at glutaminergic synapses. 24) The following is NOT true about Rous Sarcoma Virus: a) It is distinguished from other retroviruses by the presence of the v-src gene, which does not play a role in viral production. b) It contains an oncogene that is a viral form of a normal cellular gene that has been evolutionarily mutated and activated. c) It injects RNA and reverse transcriptase into cells upon infection. d) It causes the loss of growth control in the host, which plays an essential role in producing viral progeny during infection. e) It uses host cell proteins to help it integrate into the host genome and produce viral proteins. 25) The following is NOT true about the signaling pathway initiated by EGF binding to the EGF receptor (EGFR). a) EGF binding stabilizes an active dimer in which EGFR autophosphorylation provides a binding site for Grb2. b) Grb2 is an adaptor protein with SH2 and SH3 domains that bridge the EGF receptor (by SH2 binding to phosphotyrosine) to GEF/Sos (through an SH3 domain- proline rich domain interaction). c) GEF/Sos stimulates the GDP/GTP exchange on Ras. d) Ras-GTP feedback regulates EGFR activation by binding to the phosphorylated kinase domain at the membrane. e) MAP (Erk) kinase, a downstream component of a protein kinase signaling cascade, phosphorylates a variety of cytoplasmic and nuclear proteins to stimulate growth. ...
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